Histamine intolerance is defined as a disequilibrium of accumulated histamine and the capacity for histamine degradation. This clinical term addresses a non-immunologically mediated pathology when histamine ingested with food is not particularly high, however its degradation is decreased. This paper aims to provide a narrative review on etiopathology, epidemiology, possible diagnostic algorithms and diagnostic challenges of histamine intolerance in children. The clinical picture of histamine intolerance in children is similar to that observed in adults apart from male predominance found in paediatric patients. Both in children and adults, a histamine-reduced diet is typically the treatment of choice. Diamine oxidase supplementation offers another treatment option. There is no symptom or test pathognomonic for histamine intolerance. Nevertheless, manifestations of chronic gastrointestinal symptoms, measurements of diamine oxidase deficits, positive results of histamine provocation tests and improvement in symptoms with histamine-reduced diet considerably increase the probability of histamine intolerance diagnosis. These factors have been included in the proposed diagnostic algorithm for histamine intolerance. In children histamine intolerance most likely co-occurs with allergies and bowel diseases, which creates an additional diagnostic challenge. As the evidence for children is poor further research is needed the determine epidemiology, validate diagnostic algorithms and establish possible treatment options regarding histamine intolerance.

Cerebral palsy (CP) results in non-progressive damage to the central nervous system, leading to functional disorders of the gastrointestinal tract and requiring enteral nutrition via gastrostomy in some patients. The aim of the study was to assess the impact of enteral nutrition on intestinal inflammation expressed by stool calprotectin and intestinal permeability determined by fecal zonulin and IFABP, and to determine whether CP affects these parameters. The study group consisted of 30 children with CP, fed enterally (Cerebral Palsy Enteral Nutrition—CPEN), and two reference groups: 24 children with CP, fed orally with a standard diet (CPC—Cerebral Palsy Controls) and 24 healthy children (HC—healthy controls). The differences between these groups and between the combined CP groups (CPG and CPEN + CPC) and HC were analyzed. Fecal zonulin, calprotectin, and intestinal fatty acid-binding protein 2 (IFABP2) levels were determined by ELISA. The concentrations of fecal calprotectin and zonulin were significantly higher in the CPEN group than in the CPC group (p = 0.012, p = 0.025). When comparing the CPG (n = 53) with the HC group (n = 24), statistically significant differences were observed for calprotectin (p = 0.000018, higher in the CPG) and IFABP (p = 0.021, higher in HC). Enteral nutrition was associated in our cohort with increased fecal calprotectin and zonulin. Children with cerebral palsy presented with increased fecal calprotectin but not increased intestinal permeability expressed by stool zonulin.

The purpose of this study was to compare the nutritional status between deltaF508 CFTR hetero- and homozygous paediatric patients with cystic fibrosis. We assessed the percentage profiles of fatty acids measured in erythrocyte membranes and the serum levels of vitamins A, D3, E and K1 in the studied groups. We also measured the weights and heights and calculated the body mass indexes (BMIs). The studied groups consisted of 34 heterozygous and 30 homozygous patients. No statistically significant differences were found in the serum vitamins or erythrocyte membrane fatty acid profiles between the hetero- and homozygous patient groups, except for heptadecanoic acid (p = 0.038). The mean percentiles of height, weight and BMI did not differ significantly between the two groups. The homozygous and heterozygous paediatric patients with cystic fibrosis were similar in terms of their nutritional statuses.

Bacteria can impact the host organism through their metabolites, with short-chain fatty acids (SCFAs) being the most important, including acetate (C2), propionate (C3), butyrate (C4), valerate (C5n), and isovalerate (C5i). This study aimed to identify the impact of enteral nutrition on SCFAs in children with cerebral palsy and to test the hypothesis that the type of nutrition in cerebral palsy affects gut SCFA levels. Cerebral palsy is a heterogeneous syndrome resulting from non-progressive damage to the central nervous system. The study group included 30 children diagnosed with cerebral palsy, receiving enteral nutrition (Cerebral Palsy Enteral Nutrition (CPEN)) via gastrostomy. The first reference group (Cerebral Palsy Controls (CPCs)) consisted of 24 children diagnosed with cerebral palsy and fed orally on a regular diet. The second reference group (Healthy Controls (HCs)) consisted of 24 healthy children with no chronic disease and fed on a regular diet. Isolation and measurement of SCFAs were conducted using gas chromatography. Differences were observed in the median contents of isobutyric acid, valeric acid, and isovaleric acid between the CPC group, which had significantly higher levels of those acids than the HC group. No differences were found between the CPEN and CPC groups nor between the CPEN and HC groups. We conclude that enteral nutrition in cerebral palsy has no influence on the levels of SCFAs.

Background/Objectives: Limited research had investigated nutritional status in patients with Cornelia de Lange Syndrome (CdLS) (OMIM 122470, 300590, 300882, 610759, 620568 and 614701). Body composition assessed via bioelectric impedance (BIA) is a particularly under-explored issue. In this cross-sectional study, we hypothesize that body composition imbalance is frequent in CdLS and may be associated with dysphagia. We aimed to determine dysphagia prevalence in CdLS. Dysphagia may be a sign or a complication of GERD (gastroesophageal reflux disease), which is the most frequent gastroenterological disorder in CdLS patients; Methods: Fourteen Polish patients with a clinical or genetic diagnosis of CdLS were included in the study. We performed body composition analysis via bioelectric impedance taking into account the phase angle (PhA) and Body Cell Mass (BCM) in patients who cooperated and were able to sit still. The patients’ caregivers completed the pediatric version of the Eating Assessment Tool (PEDI-EAT-10). Based on the questionnaire scoring, we divided the patients into dysphagic and non-dysphagic groups. Body compartments of those two groups were compared. Statistical correlations between PhA and the PEDI-EAT-10 score were calculated; Results: Eleven of the fourteen CdLS patients had abnormalities in the BIA analysis in terms of fat mass (FM), fat free mass (FFM) and skeletal muscle mass (SMM). Six patients had excessive FM and four patients were deficient in FM. Two had deficiency in FFM and two had excessive FFM. We noted prevalence of dysphagia at 28.57%, with four patients having an PEDI-EAT-10 score higher or equal to 3, categorized as dysphagic. The dysphagic and non-dysphagic groups were not significantly different in terms of the proportion of patients with FM, FFM, SMM and BCM in the small cohort presented here. A statistically significant inverse correlation was found between the PhA and PEDI-EAT-10 score (rho = −0.72; p = 0.003); Conclusions: CdLS patients require investigation for dysphagia and nutritional status imbalance, as they are both frequent in this syndrome. The most prevalent are abnormalities in FM, both excess and deficit. PhA deviations observed in the bioimpedance study deepen with the severity of dysphagia. These findings require further investigation in a larger cohort.